In the next series of experiments, we examined whether the fast-acting opioid agonist fentanyl would exhibit a similar pharmacological profile with regard to Ca2+ channel inhibition. Figure 4 shows the time course of peak Ca2+ current inhibition in 118AA (Figure 4A) and 118GG (Figure 4C) neurons before and during fentanyl (10 μM) application. Ca2+ channel currents were evoked with a 50 ms test pulse to -15 mV from a holding potential of -80 mV applied every 10 s. The traces shown in Figure 4B and Figure 4D correspond to the numbers for 118AA and 118GG neurons, respectively. As described for morphine above (see Results, page 12, first paragraph) in 118AA neurons, exposure to fentanyl led to a 52% (Figure 4A) and 61% (Figure 4C) inhibition of Ca2+ currents. It can be seen that following fentanyl removal the period of recovery was longer when compared to that observed with morphine (cf. Figure 3A and Figure 3C). Figure 4E is a plot that compares the fentanyl concentration-response relationships for 118AA (●) and118GG (▲) neurons. The data points were also fitted to the
